Vinay L, Brocard F, Fellippa-Marques S, Clarac F
CNRS, UPR Neurobiologie et Mouvements (UPR 9011), Marseille, France.
J Physiol Paris. 1999 Sep-Oct;93(4):359-67. doi: 10.1016/s0928-4257(00)80063-7.
Presynaptic inhibition of primary afferents can be evoked from at least three sources in the adult animal: 1) by stimulation of several supraspinal structures; 2) by spinal reflex action from sensory inputs; or 3) by the activity of spinal locomotor networks. The depolarisation in the intraspinal afferent terminals which is due, at least partly, to the activation of GABA(A) receptors may be large enough to reach firing threshold and evoke action potentials that are antidromically conducted into peripheral nerves. Little is known about the development of presynaptic inhibition and its supraspinal control during ontogeny. This article, reviewing recent experiments performed on the in vitro brainstem/spinal cord preparation of the neonatal rat, demonstrates that a similar organisation is present, to some extent, in the new-born rat. A spontaneous activity consisting of antidromic discharges can be recorded from lumbar dorsal roots. The discharges are generated by the underlying afferent terminal depolarizations reaching firing threshold. The number of antidromic action potentials increases significantly in saline solution with chloride concentration reduced to 50% of control. Bath application of the GABA(A) receptor antagonist, bicuculline (5-10 microM) blocks the antidromic discharges almost completely. Dorsal root discharges are therefore triggered by chloride-dependent GABA(A) receptor-mediated mechanisms; 1) activation of descending pathways by stimulation delivered to the ventral funiculus (VF) of the spinal cord at the C1 level; 2) activation of sensory inputs by stimulation of a neighbouring dorsal root; or 3) pharmacological activation of the central pattern generators for locomotion evokes antidromic discharges in dorsal roots. VF stimulation also inhibited the response to dorsal root stimulation. The time course of this inhibition overlapped with that of the dorsal root discharge suggesting that part of the inhibition of the monosynaptic reflex may be exerted at a presynaptic level. The existence of GABA(A) receptor-independent mechanisms and the roles of the antidromic discharges in the neonatal rat are discussed.
在成年动物中,初级传入神经的突触前抑制至少可从三个来源诱发:1)通过刺激几个脊髓上结构;2)通过感觉输入的脊髓反射作用;或3)通过脊髓运动网络的活动。脊髓内传入神经末梢的去极化至少部分归因于GABA(A)受体的激活,其幅度可能大到足以达到放电阈值并引发动作电位,这些动作电位可逆向传导至外周神经。关于突触前抑制的发育及其在个体发育过程中的脊髓上控制,人们了解甚少。本文回顾了近期在新生大鼠体外脑干/脊髓制剂上进行的实验,结果表明新生大鼠在一定程度上存在类似的组织形式。可从腰段背根记录到由逆向放电组成的自发活动。这些放电是由潜在的传入神经末梢去极化达到放电阈值产生的。当氯化物浓度降至对照的50%时,在盐溶液中逆向动作电位的数量显著增加。浴用GABA(A)受体拮抗剂荷包牡丹碱(5 - 10 microM)几乎完全阻断逆向放电。因此,背根放电是由氯化物依赖性GABA(A)受体介导的机制触发的;1)通过刺激脊髓C1水平的腹侧索(VF)来激活下行通路;2)通过刺激相邻背根来激活感觉输入;或3)运动中枢模式发生器的药理学激活可诱发背根中的逆向放电。VF刺激也抑制了对背根刺激的反应。这种抑制的时间进程与背根放电的时间进程重叠,表明单突触反射的部分抑制可能在突触前水平发挥作用。本文还讨论了新生大鼠中不依赖GABA(A)受体的机制的存在以及逆向放电的作用。